Taurine (2-aminoethane sulfonic acid) is an abundant but poorly understood amino acid in the heart. Cardiac content is maintained by a specific transport process rather than by biosynthesis. Adrenergic stress causes a stimulation of the transport process in normal and stressed states. The physiological and pharmacological actions of taurine on the heart are mediated via modulations in calcium fluxes and pool sizes. The mechanism of this modulation will be examined. Experimental preparations will be the isolated, perfused Langendorff and working rat hearts and cardiac plasma membrane and sarcolemma. Defects in taurine regulation may be involved in the pathogenesis of the cardiomyopathy which is a prominent feature of Friedreich's ataxia. The cardiomyopathic Syrian hamster has a number of features in common with Friedreich's ataxia cardiomyopathy. This animal will be used as an experimental model for the devising of a pharmacological treatment for this disease. This study is concerned with linking together two mechanisms that control calcium movement in the heart cell (sympathetic nervous system and taurine). It is aimed at an understanding of the precise nature of cardiac responses to stress at the molecular level.